Our studies on the susceptibility to audiogenic seizures (AuSz), which regularly develop 24 hr after subjecting Sprague-Dawley rats to cardiac arrest cerebral ischemia (CACI), revealed a correlation in a chronological profile between onset of seizures, changes affecting the GABAergic terminals and loss of GABAA inhibition in the hippocampus as assayed by paired-pulse stimulation (PPS) testing. The cessation of susceptibility to AuSz approximately 1 month after ischemia appears to coincide with vigorous sprouting and new formation of GABAergic terminals and return of the PPS to a normal pattern. Studies on defining sites and mechanisms of GABAergic disinhibition are associated with evaluation of how much seizures may contribute to ischemic injury.